The pathophysiology of hyperkinetic movement disorders is incompletely understood. This lack of knowledge is an obstacle to the development of better symptomatic therapies. We will explore the pathophysiology of hyperkinetic movement disorders using emission tomography with ligands aimed at striatal muscarinic cholinergic receptors striatal dopaminergic terminals and striatal cholinergic terminals. We hypothesize that dystonias are characterized by excessive striatal cholinergic neurotransmission and downregulation of striatal cholinergic receptors. We predict decreased muscarinic cholinergic receptor binding with normal striatal cholinergic innervation and will test this hypothesis using [11C]N-methylpiperidyl benzilate (NMPB) to measure striatal muscarinic cholinergic receptors and (-)-5-[123I]iodobenzovesamicol to measure striatal cholinergic terminals, respectively. In Tourette's syndrome, we hypothesize that there is excessive striatal dopaminergic innervation and excessive striatal cholinergic neurotransmission. We predict increased density of striatal dopaminergic terminals and decreased striatal cholinergic receptor binding. We will test these predictions with [11C]dihydrotetrabenazine (DTBZ) and [11C]NMPB. We hypothesize that the degree of dopaminergic innervation is an important determinant of the type of movement disorder suffered by Huntington's disease patients with marked rigidity resulting from degeneration of dopaminergic neurons. We will test this hypothesis by correlating character of the movement disorder with the results of [11C]DTBZ scans. We predict significantly diminished [11C]DTBZ binding in rigid but not in choreic Huntington's disease patients.